Genetic dissection of cell wall defects and the strigolactone pathway in Arabidopsis

• Published in: Plant Direct
• Main Authors: Ramírez, Vicente, Pauly, Markus
• Other Authors: Deutsche Forschungsgemeinschaft
• Format: Article in Journal/Newspaper
• Language: English
• Published: Wiley 2019
• Subjects: eskimo*
• Online Access: http://dx.doi.org/10.1002/pld3.149; https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1002%2Fpld3.149; https://onlinelibrary.wiley.com/doi/pdf/10.1002/pld3.149; https://onlinelibrary.wiley.com/doi/full-xml/10.1002/pld3.149

Abstract Defects in the biosynthesis and/or deposition of secondary plant cell wall polymers result in the collapse of xylem vessels causing a dwarfed plant stature and an altered plant architecture termed irregular xylem ( irx ) syndrome. For example, reduced xylan O ‐acetylation causes strong developmental defects and increased freezing tolerance. Recently, we demonstrated that the irx syndrome in the trichome birefringence‐like 29/eskimo1 ( tbl29/esk1 ) mutant is dependent on MORE AXILLARY GROWTH 4 ( MAX 4), a key enzyme in the biosynthesis of the phytohormone strigolactone ( SL ). In this report, we show that other xylan‐ and cellulose‐deficient secondary wall mutants exhibit increased freezing tolerance correlated with the irx syndrome. In addition, these phenotypes are also dependent on MAX 4, suggesting a more general interaction between secondary wall defects and SL biosynthesis. In contrast, MAX 4 does not play a role in developmental defects triggered by primary wall deficiencies, suggesting that the interaction is restricted to vascular tissue. Through a reverse genetics approach, the requirement of different components of the SL pathway impacting the irx syndrome in tbl29 was evaluated. Our results show that the tbl29 ‐associated irx phenotypes are dependent on the MAX 3 and MAX 4 enzymes, involved in the early steps of SL biosynthesis. In contrast, this signaling is independent on downstream enzymes in the biosynthesis and perception of SL such as MAX 1 and MAX 2.